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Cardiorespiratory 2 PBL > PBL 7 > Flashcards

PBL 7 Flashcards

1
Q

define pulses alternans

A

this is a physical finding with arterial pulse waveform showing alternating strong and weak beats, almost always indicative of left ventricular systolic impairment and carries a poor prognosis, there is one weak beat and one strong beat, can occur in hypertension, aortic stenosis, coronary atherosclerosis and dilated cardiomyopathy

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2
Q

define hepatojugular reflux

A

this is distension of the jugular vein induced when applying manual pressure over the liver, patients torso should be at 45 degree angle, can be seen in TR, cardioic tamponade, right heart side failure

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3
Q

how does heart failure happen

A
  1. Systolic heart failure – so the heart cannot pump hard enough
  2. Diastolic heart failure – reduced preload to the heart
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4
Q

why is congestive heart failure called congestive heart failure

A

fluid backs up into the lung and can cause fluid overload this is why it is also called congestive heart failure

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5
Q

how does systolic heart failure happen

A
  • Heart needs to give out the CO per minute
  • CO = bpm x stroke volume
  • LV 70ml in stroke volume
  • Can cause a reduce in CO
  • Anything less than 40ml or less is considered HF
  • Have decreased stroke volume and increased residual volume
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6
Q

how does diastolic heart failure happen

A
  • Stroke volume is low but ejection fraction is normal, this is because although it is not filling enough it is pumping out what is normal in terms of a fraction
  • Due to reduced preload
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7
Q

describe the starling mechanism

A
  • Increased preload causes increase force of contraction

- Cardiac muscle can fail when it gets to a certain point

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8
Q

what are cardiac causes of heart failure

A
  • Bicuspid aortic valve
  • Valvular heart disease
  • Ischemic heart disease
  • Hypertension
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9
Q

what are non cardiac causes of heart failure

A
  • Infection
  • Overactive thyroid
  • Anaemia
  • Renal failure
  • Medication and drugs
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10
Q

how would diagnose heart failure

A
  • Echocardiogram – pictures of the heart using an ultrasound probe
  • ECG
  • Stress test
  • Blood tests
  • Chest x ray
  • CT
  • Coronary angiogram
  • Biopsy
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11
Q

explain her signs and symptoms

A
  • Tiredness – left ventricle cannot pump enough blood when higher O2 is required on exertion thus she exhibits tiredness,
  • Shortness of breath especially at night – reduced gas exchange from the alveoli to the blood, this is increased when laying down due to an increase in PVS, the respiratory drive being reduced when sleeping, less sympathetic bronchodilation
  • Swollen ankles which are worse in the evenings
  • Wakes up after a couple’s hour sleep – pulmonary oedema and hypoxia is more sever that they trigger waking up
  • Sleeps with several pillows
  • 160/95 hypertension
  • 122 bpm tachycardia – compensation by the sympathetic nervous system in order to increase the stroke volume that has been reduced
  • Pulsus alternas – shows left systolic impairment, they could have aortic stenosis which has lead to the left sided heart failure
  • Systolic mumrus in her chest – either aortic stenosis or mitral regurigitation
  • Crackles in the base of both her lungs – this is due to pulmonary oedema, this is caused by blood entering from the pulmonary arteries into the intersitial tissues resulting in fluid build up in her alveoli
  • Ankles are slightly swollen – right heart side failure, the fluid is going back from the heart into the body, reduced stroke volume, leads to rasied central venous pressure, starlings law has failed, worse in the evenings due to gravity
  • Hepatojugular reflux – sing of raise central venous pressure and right heart side failure
    She has both left and right sided heart failure, began in the left and was passed on to the right
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12
Q

what are the key features of left sided heart failure

A

increased end systolic volume, increased left atrial pressure, increased pulmonary venous

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13
Q

what are the key features for right sided heart failure

A

Right heart failure = PO and hypoxia cause raised central venous pressure because of increased raised pulmonary arterial pressure and pulmonary arterial constriction (causes right ventricle enlarges).

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14
Q

describe what Non-dihydropyridine calcium channel blockers do

A

verparmil
dilitizem

Selective for calcium channels in the myocardium in order to decrease heart rate and decrease force of contraction in order to decrease oxygen demand

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15
Q

describe what dihydropyriidine calcium channel blockers do and what are the side effects

A

amlodipine and nifedipine

Selective for calcium channels in the vessels in order to cause vasodilation and decrease the TPR

other drugs can cause reflexive tachycardia and hypotension and syncope

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16
Q

describe nitrates

  • examples
  • mechanism of action
  • side effects
A

GTN, Isosoribide (longer acting)

NO causes cGMP rise in smooth muscle which activates myosin light chain phosphatase via cGMP dependent protein kinase thus causes vasodilation ( it causes the dephosphorylation of myosin light chain kinase)

Headache, flushing, tachy/bradycardia
Tolerance to isosorbide can develop

Sublingual or spray is very fast acting

17
Q

describe nicroandil

  • mechanism of action
  • side effects
A

Acts as a nitrate and also opens potassium channels which hyperpolarises the cell and prevents opening of voltage gated calcium channels so net effect is vasodilation.

Flushing, palpitation, GI ulceration

Useful for nitrate tolerance

18
Q

describe beta blockers

  • examples
  • mechanism of action
  • side effects
A

Atenolol (selective B2 antaogonsit)
Propanolol (non-selective beta antagonist)

Binds to B2 receptors in the heart decreasing the heart rate and force of contractility, this can increase the end-diastolic volume

Propranolol should not be given for patients who have asthma as it can cause bronchoconstriction
Lethargy
May cause type 2 diabetes

19
Q

describe ACE/ARB

  • mechanism of action
  • side effects
A

Prevents angiotensin I being converted to angiotensin II by blocking the ACE, this prevents angiotensin II binding to an AT1 receptor on smooth muscle and prevents calcium entry which can cause vasodilation

ACE – cough, angioedema, shouldn’t be given to patients of an afrocarbbeian background
ARB is better in this instant

20
Q

describe diuretics such as furosemide

- mechanism of action

A

Remove the amount of fluid present in the heart reduce preload therefore reduce the contractile force and oxygen demand of the heart

21
Q

what are the surgical treatments available

A
  • CABG
  • Valve replacement
  • Ventricular restoration
  • ICD
  • Heart transplant
22
Q

what are the non surgical and non pharmacological treatments available

A
  • Cardiac rehab
  • Weight loss
  • Sodium fluid restriction
  • Oxygen
23
Q

what are the risks of hear failure

A
  • Diabetes
  • Smoking
  • Obesity
  • Family history
  • Air pollution
  • Hypertension
  • Cholesterol
  • Age
24
Q

what would a chest x ray look like

A
  • Heart should be enlarged – cardiomegaly
  • Kurly B lines – interstitial oedema
  • Pulmonary oedema
  • Upper lobe diversion
  • Pleural effusion – blunted costophrenic lines
25
Q

what would an echocardiogram look like

A
  • Poor ventricular function
  • Dilated chambers
  • Maybe some regurgitation
  • Por valve disease
26
Q

what would an ECG look like

A
  • Pathological Q waves
  • Bundle branch block pattern – prolonged QRS
  • Left or right sided heart deviation
27
Q

what is the expectancy of someone with heart failure

A
  • Life expectancy is poor
  • Depends on severity
  • If no patient life expectancy of 5 years is less than 50%

Death

  • Patients with ventricular function – high risk of developing ventricular arrhythmias
  • Decreasing exercise tolerance
  • Hypotension and renal function can be a caused
28
Q

describe what you would hear in a clinical examination

A
  • Small pulse volume
  • Raised venous pressure
  • Heart = left ventricular enlargement therefore there should be a displaced apex beat
  • Possible third and fourth heart sounds S3 rapid filling in systolic dysfunction S4 for forceful contraction of the atria to overcome a hypertrophic ventricle before S1
  • Pan systolic murmur – due to mitral regurgitation dilation of mitral valve ring because of LVH
29
Q

what can cause left sided heart failure

A

Systolic left sided heart failure
- Hypertrophy due to long standing hypertension so ventricle can pump ith more force, this increases oxygen demand but there is reduced demand so the ventricle muscle has weaker contraction and this can lead to failure
- Dilated cardiomyopathy – ventricle dilates and grows in size due to increased prealod, this can stretch out the muscle walls and they get thinner and weaker and this can then cause systolic left sided failure
Diastolic left sided heart failure
- Cocnentretic hypterophy – less room for blood so less CO
- Aortic stenosis – narrowing of the arotic valve opening
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy – heart muscle gets stiffer and less complaint, cant stretch out and fill enough blood
- Decreased blood flow to the kidney = activates RRA causes fluid rentention, increases preload and contraction strength, can lead up to fluid buildup in the lungs

30
Q

what can cause right sided heart failure

A
  • Usually caused by Left sied heart failure
  • Fluid build up in the pulmonary artery makes it harder for right ventricle
  • Left to right cardiac shunt such as an ASD or VSD that allows blood to flow from high pressure left side to low pressure on right side
  • Leads to concentric hypertrophy on the right ventricle, leading it to be prone to systolic dysfunction
  • Chronic lung disease – hard to exchange O2 thus in response to hypoxia the pulmonary arterioles constrict which raise the pulmonary pressure, leads to hypertrophy and failure
  • With RSF blood is backed up to the body, gets jugular venous distension, it becomes large and distended in the neck
  • Can cause hepatosplenomegaly then leads to cirrhosis and liver failure
  • Can cause pitting oedema
31
Q

why don’t patients take there medication

A
  • Common with patients who have chronic conditions
  • Fear – frightened of side effects or have witnessed side effects by someone else or on themselves
  • Cost
  • Misunderstanding – do not see the need, or the nature of the side effects
  • Too many medication
  • Lack of symptoms – don’t get the symptoms so they stop taking the medication
  • Worry – about being too dependent on medicine
  • Depression – patients who are depressed less likely to take the medication
  • Mistrust

Cardiorespiratory 2 PBL (10 decks)

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